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Cancer Biology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Interphase

A

Nucleus is visible and cell function occur

G1, S, G2

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2
Q

G1

A

btw cytokinesis and S phase
Chr are single
new organelles are formed
cell grows in size

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3
Q

Restriction point

A

G1-S transition
commitment to DNA replication and division
Can put cell in G0

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4
Q

G0

A

Resting phase. Quiescent or Senescent

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5
Q

Quiescent

A

Reversible. lack of cell growth signals
growth inhibitory signals (TGFBeta)
DNA dmg detected by p53

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6
Q

Senescent

A

Irreversible. telemoere shortening

still can function. alt to apop

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7
Q

S phase

A

DNA replicates

Sister chromatid remain together

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8
Q

G2

A

Prepares for mitosis

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9
Q

M phase

A

Mitosis

Prophase, metaphase, anaphase, telophase

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10
Q

G1/S

A

DNA damage checkpoint: S phase blocked

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11
Q

G2/M

A

checks if replication is complete

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12
Q

SAC

A

Anaphase blocked if chromatds are not properly assembled on mitotic spindle

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13
Q

CDKs

A

Cyclin dependent protiens
Ser/Thr
activated by binding to cyclin

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14
Q

CK4/6

A

Cyclin D - G1 pase

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15
Q

CDK2

A

Cyclin E - G1/S

Cyclin A - S

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16
Q

CDK1

A

Cyclin A - S/G2

Cyclin B - M

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17
Q

Inhibitors for CDK-Cyclin Activity

A

D-CDK4/6 = p16,p15,p18,p19

Cyclin E,A,B = p21,p27,p21

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18
Q

TGF beta

A

Induces p15 and p21

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19
Q

p53

A

inhibits through p21

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20
Q

pRb

A

inhibits cell cycle at R pt - binds to E2F
extensive phosphorylation of RB allows cell cycle progression
Cyclin D-CDK and Cyclin E-CDK control phosphorylation

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21
Q

Mitosis promoting Factor (MPF)

A

G2-M transition
Cyclin B combines with CDK1 = MPF
reaches critical lvl at end of G2 and counts to peak through M
Activates Anaphase promoting complex (AC/C)

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22
Q

SAC

A

Spindle assemble checkpoint

INhibits APC/C until CHR aligned on metaphase plate and checks kinetochores

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23
Q

4 modes of cell singaling

A

Endocrine = insulin
Paracrine = GF
Synpatic = AcH
Contact Dependent = Notch

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24
Q

Growth Factors

A

molecules released by cell that signal other cells

promote differentiation and maturation

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25
Q

Cytokines

A

proteins involved in immune response

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26
Q

Hormones

A

proteins, steriods, fatty acid derivatives produced by endocrine glands (long range)

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27
Q

Enzyme - coupled receptors

A

act as enzymes/ assosiate with enzymes in the cell
Control cell growth, proliferation, differentiation, survival
Ligands

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28
Q

Receptor - Tyrosine kinases (RTKs)

A

enzyme coupled
3 domains = Extracellular, Transmembrane, Cytoplasmic
Activates Ras, PI-3K

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29
Q

Dimer

A

2 receptor molecules associate

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30
Q

PI-3K signlaing

A

promotes cell survival

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31
Q

PI-3K works

A

1) PI3K binds to RTK and phosphorylates
2) PI-33k Phosporylates PIP2 which makes PIP3
3) PIPs recruit Akt and PDK1
4) PDK1 and mTor phosphorylate Akt
5) Akt released into cytosol where activates other intracellular proteins
6) Akt activates Bad, pro-apoptotic protein
7) Bcl2 released and promotes cell survival

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32
Q

PTEN

A

dephosphorylates PIP3
Tumor Supressor
men with prostate cancer have lost this

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33
Q

Mechanisms for targeting growth factor receptors

A

Downstream pathways
anti-ligand
Anti receptor
Receptor inhibitor

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34
Q

Anti ligand

A

use antibodies to target ligand

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35
Q

Anti receptor

A

use antibodies target the RTK

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36
Q

Receptor inhibitor

A

molecule inhibitor of RTK to reduce activity

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37
Q

HER2

A

gene encoding for RTK

overexpressed in breast cancer

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38
Q

Herceptin (traztuzibmab)

A

HER2 therapy
blocks downstam HER2
Flags HER2+ cells for destruction

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39
Q

Signal diversity

A

receptors activate multiple intracellular pathways

multiple effects of one signal receptor

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40
Q

Cross talk

A

pathways regulated by other pathways

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41
Q

Redundancy

A

pathways activated by more than one receptor

Diff signals but similar effects

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42
Q

Signal amplification

A

multiple steps in pathway allows for signal to be amplified

small amt of ligand = big effects

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43
Q

Apoptosis

A 
programmed cell death/cell suicide
Orderly
cells into parcels
plasma memb remains inact
recycle parts
Reponse to genomic dmg
anoxia
signaling imbalances
44
Q

Atrophy

A

too much cell death

Parkinson’s and alzheimer’s

45
Q

Hyperplasia

A

Not enough cell death

Cancer

46
Q

Necrosis

A

response to toxxic chemical/physical injury
messy
leaks cellular components
causes immune response

47
Q

Morphological changes in apoptosis

A

Pyknosis
memb blebbing
rounding of cell
reduction of cell vol

48
Q

Pyknosis

A

chromatin condensation

nucleus collapsed into dense structure due to chromatin condensation

49
Q

Anoxia

A

oxygen deprivation

50
Q

Blebs

A

patches of plasma memb extrude

51
Q

Apoptotic bodies

A

cell broken up into small fragments

Memb bound

52
Q

Phophatidylserine

A

membrane protein flips out from inner layers, signals macrophage

53
Q

3 pathways lead to apoptosis

A

Extrinsic - death ligand
Intrinsic - radiation,toxins
Perforin/granzyme - cytotoxic t cells

54
Q

Caspasses

A

family of cysteine aspartyl-specififc protease enzymes that cleave proteins after an aspartic acid

55
Q

Initiator

A

initiate apaoptosis by cleaving other caspases

56
Q

Executioner

A

cleave multiple structural and repair proteins

57
Q

Bcl2 Family protiens

A

Pro apoptotic
Pro survival
fate of cell determined by these

58
Q

Pro-Apoptotic

A

promote release of cytochrome c from mitochondria

59
Q

Pro-Survival

A

block release of cytochrome c from mitochondria

60
Q

Apoptosome

A

complex of cytochrom c and Apaf-1

Activates caspase-3

61
Q

Cancer reciprocal translocations

A

Between chromosomes 14 and 18

causes BCL-2 to come under control of constitutive promotor

62
Q

Treatment of Apaptosis in cancer

A

Bcl-2 inhibitors
p53 activation
IAP inhibitors

63
Q

Potential threats to geonme stability

A 
Errors by DNA pol
Errors by MMR enzy
Double strand breaks
Incorporation of chemically altered nucleotides
Attack from mutatgens
Defects in DNA repair
64
Q

Mismatch repair enzymes

A

monitor recently synthesized DNA to detect errors

65
Q

Satellite

A

highly repeated sequences 100+ nuc

66
Q

Microsatellites

A

highly repeated sequences that are short

67
Q

Microsatellite Instability

A

expansion or shrinkage in regions of repeated nucleotides

68
Q

Replication fork

A

Vulnerable to breakages

Considered a DB strand break even when one strand breaks only

69
Q

Exogenous Mutagens

A

Reactive oxygen species
Superoxide ions
Hyrdrogen peroxise
radicals

70
Q

Depurination

A

spontaneous loss of purine base

71
Q

Depyrimidination

A

spontanrous loss of pyrimidine

72
Q

Deammination

A

Loss of amine group protrudine from guanine adenine and cytosine

73
Q

Transition Mutation

A

one pyrimidine replaces another pyrimidine

74
Q

Transversion

A

putine replacing pyrimidine vice versa

75
Q

UV irradiation

A

produces cross links between adjacent pyrimidine bases

76
Q

Alkylating agents

A

add alkyl group through covalent attachment
Used as chemotherapy
destabilizes bonds

77
Q

DNA adducts

A

Chemical entity formed after reaction of carcinogen with DNA base

78
Q

Aflatoxin B1 (AFB1)

A

Exogenous carcinogen produced by molds

79
Q

Heterocyclic Amines

A

Arise from cooking foods at high temperatures

80
Q

Defenses against mutagens

A

Physical shield
Enzymes including superoxide dismutase
repair enzymes
Free radical scavengers (vitamin C)

81
Q

Repair Enzymes fix altered DNA

A

Dealkylating enzyme
Base excision repair
Nucleotide excision repair

82
Q

Error prone repair

A

occurs when DNA replication fork encounters a still unrepaired DNA lesion

83
Q

dsDNA repair

A

Homologydirected repair

Nonhomologous end joining

84
Q

Caretakers

A

maintenance of genomic integrity

85
Q

Gate-keepers

A

Tumor Supressors

86
Q

BRCA

A

germline mutations that increase risk of cancer
Chromosomal trnaslocations
Chromatid breaks
Triradial chromosomes

87
Q

Chromosome Instability

A

Changes in chromosome number

88
Q

Merotelic Attachment

A

kinetochore attached to two spindle poles

89
Q

Centrosomes

A

organize microtubules in mitotic spindle commonly amplified in cancer cells
Targeting these can kill cancer cells

90
Q

Tumor Progression

A

process by which normal cells evolve with increasingly neoplastic phenotypes

91
Q

Multistep tumorigenesis

A

concept that carcinogenesis takes place in discrete stepes

92
Q

Andeonmas (polyps)

A

precursors to carcinoma

93
Q

Familial adenomatous polposis (FAP)

A

if have = colon carcinoma

Inherit mutation in TS APC on chr 5

94
Q

P and Q arms

A

Submetacentric
Metcentric
Telocentric
Acrocentric

95
Q

Field Cancerization

A

Multiple apperently independent tumor arise in same organ
Sep. by normal epithelium
Poised for cancer prog

96
Q

Tumorigenesis

A

Succession of clonal expansions

97
Q

Darwininan Evolution

A

Individual cells compete with one another
random mutations create variation
FAvor proliferation and survival

98
Q

Stochastic/Clonal Evolution model

A

Accumilation of mutations enhances resistance and fitness of tumor cells
All cells have similar chance in becoming a tumor

99
Q

Intra-Tumor Heterogeneity

A

Tumor genomes become increasingly unstable

Rate of mutation soars with each gen

100
Q

Cancer Stem Cell Model

Hierarchical Model

A

Some types of cancer have subpopulation of stem cells in tumor
Stem cells are not differentiated and are capable of self renewal
Stem cells can induce tumor similar to themselves

101
Q

5 Pathway alterations

Human cells highly resistant to transformation

A 
Pathway
Ras
pRb
p53
Telomeres
PP2A
102
Q

Driver mutations

A

give cell growth advantage

103
Q

Passenger mutations

A

other mutations already in the cell

104
Q

Skin carcinoma in mice

A 
Initiator = stable long live mark
Promoter = repeat exposures cause inc prolif and is dose depenent
105
Q

Tumor Latency

A

Time btw initiation and development of detectable tumor

106
Q

Tumor promoters

A

Chronic inflamation

Mitogenic agents

107
Q

Complete Carcinogens

A

Act as initiator and promoter

Cancer Biology (2 decks)

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